Open AccessDysmetabolic mechanisms of preeclampsia development
Author(s) -
И. С. Липатов,
Yu. V. Tezikov,
A. R. Azamatov
Publication year - 2020
Publication title -
ožirenie i metabolizm
Language(s) - English
Resource type - Journals
eISSN - 2306-5524
pISSN - 2071-8713
DOI - 10.14341/omet12330
Subject(s) - pregnancy , hyperinsulinemia , medicine , preeclampsia , insulin resistance , metabolic syndrome , endocrinology , endothelial dysfunction , eclampsia , adipose tissue , physiology , diabetes mellitus , biology , genetics
Background : An in-depth study of dismetabolic mechanisms in the genesis of pre-eclampsia (PE) has been updated because pregnancy is considered as a natural model of metabolic syndrome (MS), as well as the metabolic disorders are important in development of essential hypertension. Aims : to reveal clinical and laboratory parallels in pregnancy complicated by PE without MS and pregnancy proceeding on the background of MS to assess the role of metabolic disturbances in the development of PE. Materials and methods : 82 women with MS were examined in the dynamics of pregnancy and were divided into 2 groups depending on the implementation of PE: group I consisted of 50 women with PE on the background of MS, group II 32 women with MS without PE. We formed group III consisting of 44 pregnant women with PE without accompanying diseases to assess the pathogenetic value of metabolic disorders in the development of PE. The IV (control) group consisted of 30 healthy women with physiological pregnancy. Metabolic, hematological parameters, hormones, markers of the proinflammatory state, endothelial hemostasiological dysfunction, decidualization and placental angiogenesis, accumulation dynamics and distribution loci of adipose tissue were determined in all pregnant women. Results : In the groups of pregnant women with PE, changes similar to MS were revealed: pronounced diabetic and atherogenic disorders with the development of pathological insulin resistance, hyperinsulinemia and leptinemia, endothelial-platelet link hyperactivation, thrombotic and inflammatory status, visceral type of fat deposition, hyperuricemia, hypersympathicotonia. It is proved that in the hierarchy of mechanisms of PE formation, placental dysfunction is a secondary alteration factor, which additionally potentiates the insulin resistance increase and the effects of structural and functional destabilization of the vascular endothelium. Conclusions : The direction of metabolic changes during pregnancy, the common development of PE and MS indicate the important role of dismetabolic mechanisms in the formation of PE.